dsRNA sensors and plasmacytoid dendritic cells in host defense and autoimmunity

被引:39
作者
Wang, Yaming [1 ]
Swiecki, Melissa [1 ]
McCartney, Stephen A. [1 ]
Colonna, Marco [1 ]
机构
[1] Washington Univ, Sch Med, Dept Pathol & Immunol, St Louis, MO 63110 USA
基金
美国国家卫生研究院;
关键词
dendritic cells; virus; systemic lupus erythematosus; autoimmunity; diabetes; Toll-like receptors/pattern recognition receptors; TOLL-LIKE RECEPTOR-3; DOUBLE-STRANDED-RNA; HERPES-SIMPLEX-VIRUS; NF-KAPPA-B; SYSTEMIC-LUPUS-ERYTHEMATOSUS; INNATE IMMUNE-RESPONSES; POLYRIBOINOSINIC-POLYRIBOCYTIDYLIC ACID; POLYINOSINIC-POLYCYTIDYLIC ACID; PATTERN-RECOGNITION RECEPTORS; DEPENDENT DIABETES-MELLITUS;
D O I
10.1111/j.1600-065X.2011.01049.x
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The innate immune system detects viruses through molecular sensors that trigger the production of type I interferons (IFN-I) and inflammatory cytokines. As viruses vary tremendously in size, structure, genomic composition, and tissue tropism, multiple sensors are required to detect their presence in various cell types and tissues. In this review, we summarize current knowledge of the diversity, specificity, and signaling pathways downstream of viral sensors and ask whether two distinct sensors that recognize the same viral component are complementary, compensatory, or simply redundant. We also discuss why viral sensors are differentially distributed in distinct cell types and whether a particular cell type dominates the IFN-I response during viral infection. Finally, we review evidence suggesting that inappropriate signaling through viral sensors may induce autoimmunity. The picture emerging from these studies is that disparate viral sensors in different cell types form a dynamic and integrated molecular network that can be exploited for improving vaccination and therapeutic strategies for infectious and autoimmune diseases.
引用
收藏
页码:74 / 90
页数:17
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